AUDIOGENIC-SEIZURE SUSCEPTIBILITY AND AUDITORY BRAIN-STEM RESPONSES IN RATS PRENATALLY EXPOSED TO ALCOHOL
AUDIOGENIC-SEIZURE SUSCEPTIBILITY AND AUDITORY BRAIN-STEM RESPONSES IN RATS PRENATALLY EXPOSED TO ALCOHOL
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DOI：
10.1111/j.1530-0277.1992.tb01406.x
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发表时间：
1992-06-01
影响因子：
3.2
通讯作者：
ABEL, EL
中科院分区：
文献类型：
--
作者：
BERMAN, RF;BEARE, DJ;ABEL, EL
出生前暴露于酒精（0%，17.5%，或35%乙醇衍生的热量）的大鼠在出生后第18至23天之一测试听源性癫痫发作的易感性，然后在5天后重新测试。产前酒精暴露并不影响听源性癫痫发作的易感性或严重性。然而，所有组在复检日的癫痫发作发生率均显著增加，表明存在引发效应。听觉脑干反应（ABR）数据表明，产前酒精暴露和声损伤（即，暴露于用于引发听源性癫痫发作的警铃）引起可测量的感音神经性听力损失，并且暴露于酒精和声创伤的组合相互作用相加，产生比单独的任何一种更大的听力损失。
Rats prenatally exposed to alcohol (0%, 17.5%, or 35% ethanol-derived calories) were tested for audiogenic seizure susceptibility on one of postnatal days 18 to 23, then retested 5 days later. Prenatal alcohol exposure did not influence audiogenic seizure susceptibility or severity. There was, however, a significant increase in seizure incidence on the retest day for all groups, suggesting a priming effect. Auditory brainstem response (ABR) data suggested that prenatal alcohol exposure and acoustic trauma (i.e., exposure to an alarm bell used for eliciting audiogenic seizures) induced measurable sensorineural hearing loss, and that the combined exposure to alcohol and acoustic trauma interacted additively to produce greater hearing loss than either alone.